Pub Date : 2026-02-20Epub Date: 2026-01-07DOI: 10.1016/j.isci.2026.114640
Akshay Bisht , Jennifer Ahn-Jarvis , Kendall Corbin , Suzanne Harris , Perla Troncoso-Rey , Peter Olupot-Olupot , Nuala Calder , Kevin Walsh , Kathryn Maitland , Gary Frost , Frederick J. Warren
African children suffering from severe acute malnutrition (SAM) have a disrupted gut microbiome and low short-chain fatty acids (SCFAs). These are linked to persistently high mortality and morbidity rates. Supplementing recovery feeding regimes with suitable fermentable carbohydrate may improve outcomes in SAM. We adapted in vitro colon models to investigate the ability of children with SAM to utilize four carbohydrate substrates: milk powders (with and without human milk-like oligosaccharides), chickpea-enriched feed, and inulin. All substrates, except inulin, were fermented to produce SCFAs. The inability to utilize inulin ex vivo, a widely used prebiotic, is attributed to low microbial diversity, enriched with Proteobacteria. Stool samples obtained after partial anthropometric recovery showed increased microbial diversity and higher levels of GH32 enzyme family, responsible for inulin metabolism. These findings can inform the design of future therapeutic feeds for the treatment of SAM, where inulin has been found ineffective during initial hospitalization. Alternative carbohydrates appear to be more effective in supporting gut recovery during both the initial and later treatment phases.
{"title":"Gut microbial diversity impacts carbohydrate fermentation by children with severe acute malnutrition","authors":"Akshay Bisht , Jennifer Ahn-Jarvis , Kendall Corbin , Suzanne Harris , Perla Troncoso-Rey , Peter Olupot-Olupot , Nuala Calder , Kevin Walsh , Kathryn Maitland , Gary Frost , Frederick J. Warren","doi":"10.1016/j.isci.2026.114640","DOIUrl":"10.1016/j.isci.2026.114640","url":null,"abstract":"<div><div>African children suffering from severe acute malnutrition (SAM) have a disrupted gut microbiome and low short-chain fatty acids (SCFAs). These are linked to persistently high mortality and morbidity rates. Supplementing recovery feeding regimes with suitable fermentable carbohydrate may improve outcomes in SAM. We adapted <em>in vitro</em> colon models to investigate the ability of children with SAM to utilize four carbohydrate substrates: milk powders (with and without human milk-like oligosaccharides), chickpea-enriched feed, and inulin. All substrates, except inulin, were fermented to produce SCFAs. The inability to utilize inulin <em>ex vivo</em>, a widely used prebiotic, is attributed to low microbial diversity, enriched with Proteobacteria. Stool samples obtained after partial anthropometric recovery showed increased microbial diversity and higher levels of GH32 enzyme family, responsible for inulin metabolism. These findings can inform the design of future therapeutic feeds for the treatment of SAM, where inulin has been found ineffective during initial hospitalization. Alternative carbohydrates appear to be more effective in supporting gut recovery during both the initial and later treatment phases.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114640"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2026-01-06DOI: 10.1016/j.isci.2025.114597
Martin Barainka , Angelina Zheleva , Angela Pérez-Cervera , Helena Villanueva , Daniel Meraviglia-Crivelli , Beatriz Moreno , Fernando Pastor
Nonsense-mediated mRNA decay (NMD) is an RNA quality control pathway that degrades transcripts containing premature termination codons (PTCs). While the role of NMD in modulating tumor antigenicity and immune evasion is increasingly appreciated, its interaction with splicing remains poorly understood. We uncover a mechanism by which the splicing modulators enhance tumor immunogenicity not only by inducing aberrant splicing events that generate neoantigens but also by suppressing NMD activity through the downregulation of SMG1. This stabilizes PTC-containing transcripts, potentially expanding the pool of neoantigens. Furthermore, we demonstrate that splicing modulation exerts enhanced cytotoxic effects in microsatellite instability (MSI) tumors, which are particularly reliant on NMD for survival. Expression analysis in patient tumors reveals correlations between SMG1 and drug-targeted splicing regulators, supporting a functional link between splicing and NMD. Together, our findings identify splicing modulators as inadvertent NMD inhibitors that simultaneously boost tumor antigenicity and can be used to selectively target NMD-addicted tumors.
{"title":"Pharmacological perturbation of splicing elicits SMG1 reduction: Implications for cancer therapy","authors":"Martin Barainka , Angelina Zheleva , Angela Pérez-Cervera , Helena Villanueva , Daniel Meraviglia-Crivelli , Beatriz Moreno , Fernando Pastor","doi":"10.1016/j.isci.2025.114597","DOIUrl":"10.1016/j.isci.2025.114597","url":null,"abstract":"<div><div>Nonsense-mediated mRNA decay (NMD) is an RNA quality control pathway that degrades transcripts containing premature termination codons (PTCs). While the role of NMD in modulating tumor antigenicity and immune evasion is increasingly appreciated, its interaction with splicing remains poorly understood. We uncover a mechanism by which the splicing modulators enhance tumor immunogenicity not only by inducing aberrant splicing events that generate neoantigens but also by suppressing NMD activity through the downregulation of SMG1. This stabilizes PTC-containing transcripts, potentially expanding the pool of neoantigens. Furthermore, we demonstrate that splicing modulation exerts enhanced cytotoxic effects in microsatellite instability (MSI) tumors, which are particularly reliant on NMD for survival. Expression analysis in patient tumors reveals correlations between SMG1 and drug-targeted splicing regulators, supporting a functional link between splicing and NMD. Together, our findings identify splicing modulators as inadvertent NMD inhibitors that simultaneously boost tumor antigenicity and can be used to selectively target NMD-addicted tumors.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114597"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146035801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2026-01-24DOI: 10.1016/j.isci.2026.114744
Feiteng Wang , Shuangshuang Liu , Lin Wang , Chunhai Xu , Hongfei Meng
Mountain glaciers, which constitute vital freshwater reservoirs for ecosystems and human populations worldwide, are undergoing accelerated retreats under anthropogenic warming. This review synthesizes current approaches to artificially mitigate glacier mass loss, focusing on two intervention categories: (1) enhancing accumulation through artificial snowmaking and water injection, and (2) limiting ablation via manual compaction and surface covering. We evaluate the physical mechanisms, operational efficacy, and environmental trade-offs of these methods, drawing on empirical implementations across diverse glacial settings—including detailed case studies from western China. While these interventions offer measurable local reductions in melt, they cannot offset large-scale cryospheric decline. We, therefore, propose a dual-pathway conservation framework that couples local technical strategies—adaptively deployed in high-priority zones—with stringent global climate mitigation, thereby supporting the preservation of glacial functions and socio-ecological resilience in a rapidly changing world.
{"title":"Mountain glacier preservation with artificial interventions: A review","authors":"Feiteng Wang , Shuangshuang Liu , Lin Wang , Chunhai Xu , Hongfei Meng","doi":"10.1016/j.isci.2026.114744","DOIUrl":"10.1016/j.isci.2026.114744","url":null,"abstract":"<div><div>Mountain glaciers, which constitute vital freshwater reservoirs for ecosystems and human populations worldwide, are undergoing accelerated retreats under anthropogenic warming. This review synthesizes current approaches to artificially mitigate glacier mass loss, focusing on two intervention categories: (1) enhancing accumulation through artificial snowmaking and water injection, and (2) limiting ablation via manual compaction and surface covering. We evaluate the physical mechanisms, operational efficacy, and environmental trade-offs of these methods, drawing on empirical implementations across diverse glacial settings—including detailed case studies from western China. While these interventions offer measurable local reductions in melt, they cannot offset large-scale cryospheric decline. We, therefore, propose a dual-pathway conservation framework that couples local technical strategies—adaptively deployed in high-priority zones—with stringent global climate mitigation, thereby supporting the preservation of glacial functions and socio-ecological resilience in a rapidly changing world.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114744"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146184974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2026-01-08DOI: 10.1016/j.isci.2025.114602
Congqi Zhu , Dan Zhu , Fengyi Liu , Ruchun Li
Joule heating technology, as an ultrafast, efficient, and scalable synthesis strategy, provides a novel approach for the preparation of high-performance electrocatalysts toward various energy conversion systems, such as hydrogen production, metal-air battery, fuel cell, and so on. This review summarizes recent progress in ultrafast synthesis strategy (especially Joule heating technology) for the precise construction of highly active electrocatalysts. First, the principle of Joule heating technology has been discussed. The fundamental electrocatalytic mechanisms, such as hydrogen evolution reaction (HER), oxygen evolution reaction (OER), overall water splitting, nitrate reduction reaction (NO3RR), oxygen reduction reaction (ORR), and carbon dioxide reduction reaction (CO2RR), are also comprehensively highlighted. The recent advances of electrocatalysts prepared by ultrafast Joule heating technology have been generalized. Furthermore, this review also addresses the inherent limitations of the Joule heating approach and outlines prospects and challenges, aiming to lay a foundation for breakthroughs and applications of Joule heating in electrocatalysis.
{"title":"Recent advances in joule heating ultrafast technology for electrocatalysis","authors":"Congqi Zhu , Dan Zhu , Fengyi Liu , Ruchun Li","doi":"10.1016/j.isci.2025.114602","DOIUrl":"10.1016/j.isci.2025.114602","url":null,"abstract":"<div><div>Joule heating technology, as an ultrafast, efficient, and scalable synthesis strategy, provides a novel approach for the preparation of high-performance electrocatalysts toward various energy conversion systems, such as hydrogen production, metal-air battery, fuel cell, and so on. This review summarizes recent progress in ultrafast synthesis strategy (especially Joule heating technology) for the precise construction of highly active electrocatalysts. First, the principle of Joule heating technology has been discussed. The fundamental electrocatalytic mechanisms, such as hydrogen evolution reaction (HER), oxygen evolution reaction (OER), overall water splitting, nitrate reduction reaction (NO<sub>3</sub>RR), oxygen reduction reaction (ORR), and carbon dioxide reduction reaction (CO<sub>2</sub>RR), are also comprehensively highlighted. The recent advances of electrocatalysts prepared by ultrafast Joule heating technology have been generalized. Furthermore, this review also addresses the inherent limitations of the Joule heating approach and outlines prospects and challenges, aiming to lay a foundation for breakthroughs and applications of Joule heating in electrocatalysis.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114602"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146185052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-08DOI: 10.1016/j.isci.2025.114365
Zhenyu Zhu , Yongcheng Liang , Xiaowen Liu , Fanqi Kong , Kaiqiang Sun , Ximing Xu , Jiangang Shi
Intervertebral disc degeneration involves loss of nucleus pulposus (NP) cells driven by inflammatory and mitochondrial stress-related death pathways. Because mitophagy maintains mitochondrial quality, its disruption may influence cell fate during degeneration. Using human tissues, a mouse lumbar instability model, a rat disc puncture model, and human NP cells stimulated with TNF-α, SM-164, and Z-VAD-FMK (TSZ), we examined how mitochondrial quality control shapes necroptotic signaling. Necroptotic cells displayed mitochondrial damage and reduced mitophagy, while mitophagy activation limited necroptosis and preserved extracellular matrix components. We identified the mitochondrial protein PHB2 as a key regulator linking mitophagy to suppression of necroptosis. PHB2 loss impaired mitophagy, disrupted mitochondrial function, and intensified necroptotic death, whereas PHB2 overexpression restored mitophagy, maintained mitochondrial membrane potential, and reduced degeneration. In vivo PHB2 delivery mitigated necroptosis and protected disc structure. These findings highlight a mitochondria-centered mechanism that shapes cell survival during disc degeneration.
{"title":"PHB2 mitigates intervertebral disc degeneration by modulating mitophagy to inhibit necroptosis in nucleus pulposus cells","authors":"Zhenyu Zhu , Yongcheng Liang , Xiaowen Liu , Fanqi Kong , Kaiqiang Sun , Ximing Xu , Jiangang Shi","doi":"10.1016/j.isci.2025.114365","DOIUrl":"10.1016/j.isci.2025.114365","url":null,"abstract":"<div><div>Intervertebral disc degeneration involves loss of nucleus pulposus (NP) cells driven by inflammatory and mitochondrial stress-related death pathways. Because mitophagy maintains mitochondrial quality, its disruption may influence cell fate during degeneration. Using human tissues, a mouse lumbar instability model, a rat disc puncture model, and human NP cells stimulated with TNF-α, SM-164, and Z-VAD-FMK (TSZ), we examined how mitochondrial quality control shapes necroptotic signaling. Necroptotic cells displayed mitochondrial damage and reduced mitophagy, while mitophagy activation limited necroptosis and preserved extracellular matrix components. We identified the mitochondrial protein PHB2 as a key regulator linking mitophagy to suppression of necroptosis. PHB2 loss impaired mitophagy, disrupted mitochondrial function, and intensified necroptotic death, whereas PHB2 overexpression restored mitophagy, maintained mitochondrial membrane potential, and reduced degeneration. <em>In vivo</em> PHB2 delivery mitigated necroptosis and protected disc structure. These findings highlight a mitochondria-centered mechanism that shapes cell survival during disc degeneration.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114365"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-29DOI: 10.1016/j.isci.2025.114572
David J. Friedman , Sina Ramin , Tiffany Blair , Gwen Kramer , Shelly Bambina , Alejandro F. Alice , Jason Baird , Terry Medler , Kristina H. Young , Marka R. Crittenden , Michael J. Gough
Radiation therapy (RT) is recognized for its ability to induce DNA damage within cancer cells, leading to cancer cell death and promotion of anti-tumor immune responses. However, this beneficial effect is often counterbalanced by the presence of suppressive Tregs. Although factors such as RT-induced transforming growth factor β (TGF-β) can contribute to increased Treg accumulation within the tumor, the dynamics of Treg movement, and recruitment in the post-RT tumor microenvironment are not fully understood. Our study examined Treg migration following RT, revealing that RT disrupts Treg migration to the tumor-draining lymph node (TdLN) and alters their phenotype. Combining RT with anti-CCR8 therapy, which selectively depletes Tregs within the tumor, significantly reduced tumor burden, and increased survival in preclinical models. This combination also proved effective against distant and unirradiated tumors. Additionally, efficacy of combination therapy was CD8 T cell dependent. These findings highlight the potential of combining RT with Treg-targeting therapies to enhance anti-tumor immunity.
{"title":"Fluorescence tracking Treg movement identifies anti-CCR8 and radiation as a therapeutic combination","authors":"David J. Friedman , Sina Ramin , Tiffany Blair , Gwen Kramer , Shelly Bambina , Alejandro F. Alice , Jason Baird , Terry Medler , Kristina H. Young , Marka R. Crittenden , Michael J. Gough","doi":"10.1016/j.isci.2025.114572","DOIUrl":"10.1016/j.isci.2025.114572","url":null,"abstract":"<div><div>Radiation therapy (RT) is recognized for its ability to induce DNA damage within cancer cells, leading to cancer cell death and promotion of anti-tumor immune responses. However, this beneficial effect is often counterbalanced by the presence of suppressive Tregs. Although factors such as RT-induced transforming growth factor β (TGF-β) can contribute to increased Treg accumulation within the tumor, the dynamics of Treg movement, and recruitment in the post-RT tumor microenvironment are not fully understood. Our study examined Treg migration following RT, revealing that RT disrupts Treg migration to the tumor-draining lymph node (TdLN) and alters their phenotype. Combining RT with anti-CCR8 therapy, which selectively depletes Tregs within the tumor, significantly reduced tumor burden, and increased survival in preclinical models. This combination also proved effective against distant and unirradiated tumors. Additionally, efficacy of combination therapy was CD8 T cell dependent. These findings highlight the potential of combining RT with Treg-targeting therapies to enhance anti-tumor immunity.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114572"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-29DOI: 10.1016/j.isci.2025.114566
Alberto Felix-Lopez , Joaquin Lopez-Orozco , Mohamed Elaish , Nawell Fayad , Zaikun Xu , Tekeleselassie Woldemariam , Bardes B. Hassan , Rashmi Panigrahi , Juveriya Qamar Khan , Megha Rohamare , Irv Mayers , J.N. Mark Glover , Joyce A. Wilson , Darryl Falzarano , Anil Kumar , Tom C. Hobman
SARS-CoV-2 is the causative agent of COVID-19, and although vaccines have reduced disease severity, emerging variants remain a significant public health issue. Broadly effective therapeutics, particularly those targeting host pathways essential for coronavirus infection, are still needed. Here, we used a CRISPR knockout screen to identify druggable host factors required for SARS-CoV-2 infection. The screen revealed NAE1 and FGFR1 as key contributors to infection. Inhibitors, either FDA-approved or those in clinical trials, of these pathways reduced replication of both ancestral and contemporary viral variants. Mechanistic studies showed that FGFR1 promotes viral replication through downstream MEK/ERK signaling, while neddylation appears to support viral entry or infectivity rather than replication itself. In a murine model of severe COVID-19, inhibitors of NAE1 and FGFR1 significantly decreased viral load and lung pathology. These findings support the development of host-targeted antiviral strategies.
{"title":"FGFR signaling and neddylation facilitate SARS-CoV-2 infection by modulating interferon induction and viral entry, respectively","authors":"Alberto Felix-Lopez , Joaquin Lopez-Orozco , Mohamed Elaish , Nawell Fayad , Zaikun Xu , Tekeleselassie Woldemariam , Bardes B. Hassan , Rashmi Panigrahi , Juveriya Qamar Khan , Megha Rohamare , Irv Mayers , J.N. Mark Glover , Joyce A. Wilson , Darryl Falzarano , Anil Kumar , Tom C. Hobman","doi":"10.1016/j.isci.2025.114566","DOIUrl":"10.1016/j.isci.2025.114566","url":null,"abstract":"<div><div>SARS-CoV-2 is the causative agent of COVID-19, and although vaccines have reduced disease severity, emerging variants remain a significant public health issue. Broadly effective therapeutics, particularly those targeting host pathways essential for coronavirus infection, are still needed. Here, we used a CRISPR knockout screen to identify druggable host factors required for SARS-CoV-2 infection. The screen revealed NAE1 and FGFR1 as key contributors to infection. Inhibitors, either FDA-approved or those in clinical trials, of these pathways reduced replication of both ancestral and contemporary viral variants. Mechanistic studies showed that FGFR1 promotes viral replication through downstream MEK/ERK signaling, while neddylation appears to support viral entry or infectivity rather than replication itself. In a murine model of severe COVID-19, inhibitors of NAE1 and FGFR1 significantly decreased viral load and lung pathology. These findings support the development of host-targeted antiviral strategies.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114566"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-23DOI: 10.1016/j.isci.2025.114247
Yuan Tang , Fei Peng , Chunyu Li , Yuqi Zhu , Xingyu Wang , Yipeng Cheng , Su Xiong , Xingwen Yu , Suixiang Li , Qidong Tai , Xinyi Yang , Huanzhang Zhu
Managing exudate is crucial for treating chronic wounds such as diabetic foot ulcers, as excess exudate can hinder healing. Traditional dressings often fall short for highly exudative or infected wounds. This study introduces an innovative alginate aerogel with nicotinamide mononucleotide (NMN)-modified Cerium Dioxide nanoparticles (CeO2 NPs). When absorbing exudate, the aerogel becomes a hydrogel, allowing controlled nanoparticle release at the wound site, preventing excess exudate buildup. The CeO2 NPs boost NMN’s effects by reducing inflammation, encouraging a shift from pro-inflammatory to anti-inflammatory macrophages, and providing strong antibacterial properties. This approach offers a promising solution for managing highly exudative diabetic foot ulcers, addressing both physical and inflammatory healing barriers.
{"title":"Nicotinamide mononucleotide modified CeO2 hydrogels promote diabetic wound healing by managing exudate and reducing inflammation","authors":"Yuan Tang , Fei Peng , Chunyu Li , Yuqi Zhu , Xingyu Wang , Yipeng Cheng , Su Xiong , Xingwen Yu , Suixiang Li , Qidong Tai , Xinyi Yang , Huanzhang Zhu","doi":"10.1016/j.isci.2025.114247","DOIUrl":"10.1016/j.isci.2025.114247","url":null,"abstract":"<div><div>Managing exudate is crucial for treating chronic wounds such as diabetic foot ulcers, as excess exudate can hinder healing. Traditional dressings often fall short for highly exudative or infected wounds. This study introduces an innovative alginate aerogel with nicotinamide mononucleotide (NMN)-modified Cerium Dioxide nanoparticles (CeO<sub>2</sub> NPs). When absorbing exudate, the aerogel becomes a hydrogel, allowing controlled nanoparticle release at the wound site, preventing excess exudate buildup. The CeO<sub>2</sub> NPs boost NMN’s effects by reducing inflammation, encouraging a shift from pro-inflammatory to anti-inflammatory macrophages, and providing strong antibacterial properties. This approach offers a promising solution for managing highly exudative diabetic foot ulcers, addressing both physical and inflammatory healing barriers.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114247"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-31DOI: 10.1016/j.isci.2025.114584
Yan Du , Zhiwei Zhang , Zhong Lin Wang , Di Wei
The environmental perception capability of embodied intelligent systems is highly dependent on their physical interactions with the surrounding environment, where tele-perception serves as a key technology enabling adaptive interaction and real-time human-machine interaction (HMI). However, existing tele-perception systems are fundamentally constrained by their underlying physical mechanisms and environmental disturbances, resulting in limited sensing directionality, poor spatial resolution, and inadequate environmental robustness. To address these challenges, this study develops an omnidirectional nano-architectured electret skin (NAES) by precisely tuning charge-trapping units within the established heterogeneous interface of the charge transport layer (CTL) and charge blocking layer (CBL). The proposed architecture arranges NAES units along 0°, 45°, 90°, 135°, and four diagonal orientations, leveraging the anisotropic electrostatic disturbance responses of each unit to achieve high-precision tele-perception of omnidirectional targets in three-dimensional space. This design overcomes the unidirectional sensing limitation of conventional NAES systems, enabling enhanced spatial perception and adaptive omnidirectional interaction in complex, dynamic environments.
{"title":"Omnidirectional tele-perception enabled by nano-architectured electret skin","authors":"Yan Du , Zhiwei Zhang , Zhong Lin Wang , Di Wei","doi":"10.1016/j.isci.2025.114584","DOIUrl":"10.1016/j.isci.2025.114584","url":null,"abstract":"<div><div>The environmental perception capability of embodied intelligent systems is highly dependent on their physical interactions with the surrounding environment, where tele-perception serves as a key technology enabling adaptive interaction and real-time human-machine interaction (HMI). However, existing tele-perception systems are fundamentally constrained by their underlying physical mechanisms and environmental disturbances, resulting in limited sensing directionality, poor spatial resolution, and inadequate environmental robustness. To address these challenges, this study develops an omnidirectional nano-architectured electret skin (NAES) by precisely tuning charge-trapping units within the established heterogeneous interface of the charge transport layer (CTL) and charge blocking layer (CBL). The proposed architecture arranges NAES units along 0°, 45°, 90°, 135°, and four diagonal orientations, leveraging the anisotropic electrostatic disturbance responses of each unit to achieve high-precision tele-perception of omnidirectional targets in three-dimensional space. This design overcomes the unidirectional sensing limitation of conventional NAES systems, enabling enhanced spatial perception and adaptive omnidirectional interaction in complex, dynamic environments.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114584"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-02-20Epub Date: 2025-12-30DOI: 10.1016/j.isci.2025.114579
Seung-Taek Park , Jina Won , Siyeon Jin , Sujin Kim , Haeun Shin , Su Hyun Lim , Ye-Ji Bang , Hyun Jik Kim
The nasopharynx (NP) serves as a primary site for localized immune responses that restrict the spread of SARS-CoV-2 to the lower respiratory tract. The microbiome is increasingly recognized as a key modulator of antiviral immunity but whether it shapes immune responses in upper airway remains uncharacterized. Detailed microbial profiles revealed that S. aureus complex abundance was the primary discriminating factor of microbial community in the NP and the enhanced abundance of S. aureus complex correlated with higher frequencies of CD4+, CD8+ tissue-resident memory T (TRM), and BRM cells. The abundance of S. aureus complex was closely associated with distinct metabolic pathways, particularly those involved in nitrogen metabolism (e.g., arginine, ornithine, and proline interconversion) and the mevalonate pathway for carotenoid biosynthesis. These findings suggest that S. aureus complex may foster unique metabolic dynamics in the NP in enhancing the tissue-residency of memory cells and localized immune responses in upper airway.
{"title":"Distinct commensal bacteria in human nasopharyngeal lymphoid tissue associated with localized immunological memory","authors":"Seung-Taek Park , Jina Won , Siyeon Jin , Sujin Kim , Haeun Shin , Su Hyun Lim , Ye-Ji Bang , Hyun Jik Kim","doi":"10.1016/j.isci.2025.114579","DOIUrl":"10.1016/j.isci.2025.114579","url":null,"abstract":"<div><div>The nasopharynx (NP) serves as a primary site for localized immune responses that restrict the spread of SARS-CoV-2 to the lower respiratory tract. The microbiome is increasingly recognized as a key modulator of antiviral immunity but whether it shapes immune responses in upper airway remains uncharacterized. Detailed microbial profiles revealed that <em>S</em>. <em>aureus</em> complex abundance was the primary discriminating factor of microbial community in the NP and the enhanced abundance of <em>S</em>. <em>aureus</em> complex correlated with higher frequencies of CD4<sup>+</sup>, CD8<sup>+</sup> tissue-resident memory T (T<sub>RM</sub>), and B<sub>RM</sub> cells. The abundance of <em>S</em>. <em>aureus</em> complex was closely associated with distinct metabolic pathways, particularly those involved in nitrogen metabolism (e.g., arginine, ornithine, and proline interconversion) and the mevalonate pathway for carotenoid biosynthesis. These findings suggest that <em>S</em>. <em>aureus</em> complex may foster unique metabolic dynamics in the NP in enhancing the tissue-residency of memory cells and localized immune responses in upper airway.</div></div>","PeriodicalId":342,"journal":{"name":"iScience","volume":"29 2","pages":"Article 114579"},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145975590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}